InUpdate: The current (November 2014) hypothesis among my doctors is that whatever they were called in my past posts — Dieulafoy lesions, Cameron’s erosions, or bleeding ulcers — all these bleeds have their source in the portal hypertension which comes from cirrhosis which is caused by my auto immune system attacking my bile ducts, that is, my primary biliary cirrhosis.
one of my posts last month, At Risk for Esophageal Varices and I Nearly Bleed Out from a Gastric Ulcer: How Weird Is That?, I raised these questions: can a burst esophageal varice adjacent to the cardia be mistaken for a spurting gastric ulcer? Is it really possible to have such an awful gastric ulcer and no abdominal pain?
I’ve since had a follow-up endoscopy, this one by my hepatologist, and will have another in a month’s time when the clips that the GI used in his repair fall off. They obscured the full view of what the hepatologist thinks may have been neither a gastric ulcer nor an esophageal varice but something else altogether: a Dieulafoy’s lesion.
So I was a just little bit right, or not altogether wrong. My gut instinct — that I couldn’t really have a gastric ulcer — may prove right, but I got caught up in the either/or fallacy: either ulcer or varices, never knowing there could be other possibilities, like this thing called Dieulafoy’s lesion.
It isn’t surprising that a Dieulafoy’s lesion could be mistaken for an ulcer, expecially when it is spurting blood.
A Dieulafoy’s lesion is an “uncommon cause of major gastrointestinal bleeding”
caused by an abnormally large-calibre persistent tortuous submucosal artery. . . The artery protrudes through a solitary, tiny mucosal defect (2-5 mm), commonly in the upper part of the stomach. It may rupture spontaneously and lead to massive bleeding. It has been suggested that the thin mucosa overlying a pulsating artery is eroded progressively by the mechanical pressure from the abnormal vessel.
So it isn’t a disease or chronic condition. It’s a mechanical failure.
Dieulafoy’s lesions and gastric ulcers can be fixed the same way. If the fix is the same, does it matter whether the problem is a Dieulafoy’s lesion or an ulcer?
I think it does because if it is a lesion and not an ulcer, I don’t have to take drugs to inhibit the development of ulcers, and I don’t have to avoid aspirin, ibupropen, and a host of other painkillers, or make dietary changes. I don’t have to worry about an ulcer recurring, either.
So why did the GI see one thing and the hepatologist another?
I’m not sure, but I suspect what we have here is another example of the simple fact that some doctors are better than others. I know there are people who don’t question doctors because they assume anyone accepted into medical school and who makes it through the training must be pretty bright. That stands to reason.
And yet. . . have a look at the night sky. All stars are bright, but some are a lot brighter than others. That might bear remembering if you have your doubts about a diagnosis.
Recognizing a Dieulafoy’s lesion depends on “awareness of the condition and experience in endoscopy.” Experience comes with time, but awareness — well, that seems to me what separates the good from the best.
Had the GI considered Dieulafoy’s lesion as an alternative to an ulcer, then I would assume the next step would be to consider what was known about my case and compare it to what is known about these lesions.
Here are some distinguishing characteristics of Dieulafoy’s lesions:
- The most common presenting symptom is recurrent, often massive, haematemesis associated with melaena (51%).
- Characteristically, there are no symptoms of dyspepsia, anorexia or abdominal pain.
- Initial examination may reveal haemodynamic instability, postural hypotension and anaemia. The mean haemoglobin level on admission has been reported to be between 8.4- 9.2 g/dl in various studies. The average transfusion requirement for the initial resuscitation is usually in excess of three and up to 8 units of packed red blood cells.
- Approximately 75% to 95% of Dieulafoy lesions are found within 6 cm of the gastroesophageal junction, predominantly on the lesser curve.
- A history of NSAID [nonsteroidal anti-inflammatory agents/analgesics] or alcohol abuse is usually absent.
Check, check, check, check, check: all true for me.